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Cylindromatosis and the CYLD gene: new lessons on the molecular principles of epithelial growth control

Massoumi, Ramin LU and Paus, Ralf (2007) In BioEssays 29(12). p.1203-1214
Abstract
Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1... (More)
Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1 expression to limit tumorigenesis, and chart how tumor growth-promoting agents or UV light and inflammatory mediators can activate CYLD. We argue that these recent insights into CYLD function and cylindroma pathogenesis may lead to the development of novel molecular strategies for cancer prevention and treatment. (Less)
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author
and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
BioEssays
volume
29
issue
12
pages
1203 - 1214
publisher
John Wiley & Sons Inc.
external identifiers
  • wos:000251526300006
  • scopus:36849035347
ISSN
0265-9247
DOI
10.1002/bies.20677
language
English
LU publication?
yes
id
40c2e067-4db2-439a-9599-fd919ee302a8 (old id 966418)
date added to LUP
2016-04-01 11:43:00
date last changed
2022-05-06 08:10:26
@article{40c2e067-4db2-439a-9599-fd919ee302a8,
  abstract     = {{Analysing cylindromatosis and the associated defects in the CYLD gene is providing novel insights into the molecular principles of epithelial growth control and carcinogenesis in, and beyond, the skin. In this review, we summarize the histopathology and histogenesis of cylindromas, and the available genetic information on patients with these skin appendage tumors. Focusing on recent data concerning the normal functions and signaling interactions of the CYLD gene product, we explain how CYLD interferes with TNF-alpha or TLR-mediated signaling as well as with JNK or NF-kappa B-dependent p65/50 signaling to limit inflammation. In addition, we delineate how CYLD interferes with activation of the proto-oncogene BCl3 and with cyclin D1 expression to limit tumorigenesis, and chart how tumor growth-promoting agents or UV light and inflammatory mediators can activate CYLD. We argue that these recent insights into CYLD function and cylindroma pathogenesis may lead to the development of novel molecular strategies for cancer prevention and treatment.}},
  author       = {{Massoumi, Ramin and Paus, Ralf}},
  issn         = {{0265-9247}},
  language     = {{eng}},
  number       = {{12}},
  pages        = {{1203--1214}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{BioEssays}},
  title        = {{Cylindromatosis and the CYLD gene: new lessons on the molecular principles of epithelial growth control}},
  url          = {{http://dx.doi.org/10.1002/bies.20677}},
  doi          = {{10.1002/bies.20677}},
  volume       = {{29}},
  year         = {{2007}},
}